Paper Information

Title:  INVESTIGATION THE ROLE OF ANGII IN REACTIVE OXYGEN SPECIES PRODUCTION AND MODULATORY ROLE OF NO IN VESSEL RESPONSES TO ANGII IN ACUTE JOINT INFLAMMATION IN THE RABBIT
Type: SPEECH
Author(s): SADEGHI N.,NAJAFIPOUR H.,GHOLAM HOSSEINIAN A.
 
 
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2007Volume 18
 
 
Abstract: 

It has been approved that NO production in most tissues increases during acute inflammation. Regulation of Joint Blood Flow (JBF) is important in this situation so the aim of this study was to investigate the interaction of local AngII and reactive oxygen species (ROS) production And the modulatory role of NO on regulation of joint blood flow during acute inflammation. The present study was performed on 24 Newzealand white rabbits divided into three experimental and one control groups. Acute knee joint inflammation was produced by intraarticular injection of 0.5ml of a 2% solution of carrageenan in knee joint. In the first group after 24 hours animals were anesthetized by thiopental sodium and carotid artery, jugular vein and saphenous artery were cannulated for recording blood pressure, injection of L-NAME, AngII and losartan respectively. Blood flow was recorded by laser Doppler flow meter. Joint vascular resistance (JVR) was calculated by dividing arterial blood pressure (ABP) by (JBF). In the second group, knee joint tissue was used for homogenization and ROS measurement. In the third group, Losartan (10mg/kg) was administrated orally 2 hours before carrageenan. JVR in response to AngII was significantly increased before and after L-NAME (P<0.01). Losartan completely blocked the effect of AngII on JVR.Total amount of antioxidant nonsignificantly increased in inflamed group and Losartan returned significantly it to the normal level (P<0.01).
Conclusion: It seems that NO plays a role in the regulation of joint vascular tone and modulates the AT1 receptor which mediates vasoconstrictor effects of AngII on these vessels. The inhibition of increase in ROS production by losartan, indicates that the production of ROS during joint inflammation is via angiotensinII and through the AT1 receptors.

 
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